White J R, Gordon-Smith E C, Rutherford T R
Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, London, United Kingdom.
Biochem Biophys Res Commun. 1996 Dec 13;229(2):504-10. doi: 10.1006/bbrc.1996.1834.
We have studied the role of Ras GTPase activating protein (GAP) in the chronic myeloid leukaemia cell line K562 by downregulating its expression using antisense RNA. This had no effect on cell proliferation and survival, suggesting that other effector molecules mediate these roles of Ras. Differentiation to macrophages following treatment with the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate was found to correlate with a significant increase in expression of GAP in K562 cells. When GAP expression was downregulated by antisense RNA, the degree of macrophage differentiation was increased, implicating GAP in the regulation of macrophage differentiation.
我们通过使用反义RNA下调Ras GTP酶激活蛋白(GAP)的表达,研究了其在慢性髓性白血病细胞系K562中的作用。这对细胞增殖和存活没有影响,表明其他效应分子介导了Ras的这些作用。在用佛波酯12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯处理后向巨噬细胞的分化,被发现与K562细胞中GAP表达的显著增加相关。当通过反义RNA下调GAP表达时,巨噬细胞分化程度增加,这表明GAP参与了巨噬细胞分化的调节。